Receptors, Adrenergic, beta
Molecular Sequence Data
Transforming Growth Factor beta
Amino Acid Sequence
Integrin beta Chains
beta 2-Glycoprotein I
Amino Acid Substitution
Receptors, Adrenergic, beta-2
Receptors, Adrenergic, beta-1
Glycogen Synthase Kinase 3
Sequence Homology, Amino Acid
Transforming Growth Factor beta1
Estrogen Receptor beta
Receptors, Adrenergic, beta-3
Protein Structure, Secondary
DNA Polymerase beta
Recombinant Fusion Proteins
Gene Expression Regulation
Dose-Response Relationship, Drug
Receptors, Transforming Growth Factor beta
Magnetic Resonance Spectroscopy
Drug-Induced Liver Injury
Amino Acid Motifs
Protein Structure, Tertiary
Electrophoresis, Polyacrylamide Gel
Tumor Necrosis Factor-alpha
Tumor Cells, Cultured
Phospholipase C beta
Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Hepatocyte Nuclear Factor 3-beta
Liver Function Tests
Hepatocyte Nuclear Factor 1-beta
RNA, Transfer, Ala
Disease Models, Animal
Promoter Regions, Genetic
Chorionic Gonadotropin, beta Subunit, Human
Islets of Langerhans
Protein Kinase C beta
Transforming Growth Factor beta2
Chromatography, High Pressure Liquid
Analysis of 4-phosphopantetheinylation of polyhydroxybutyrate synthase from Ralstonia eutropha: generation of beta-alanine auxotrophic Tn5 mutants and cloning of the panD gene region. (1/407)The postulated posttranslational modification of the polyhydroxybutyrate (PHA) synthase from Ralstonia eutropha by 4-phosphopantetheine was investigated. Four beta-alanine auxotrophic Tn5-induced mutants of R. eutropha HF39 were isolated, and two insertions were mapped in an open reading frame with strong similarity to the panD gene from Escherichia coli, encoding L-aspartate-1-decarboxylase (EC 184.108.40.206), whereas two other insertions were mapped in an open reading frame (ORF) with strong similarity to the NAD(P)+ transhydrogenase (EC 220.127.116.11) alpha 1 subunit, encoded by the pntAA gene from Escherichia coli. The panD gene was cloned by complementation of the panD mutant of R. eutropha Q20. DNA sequencing of the panD gene region (3,312 bp) revealed an ORF of 365 bp, encoding a protein with 63 and 67% amino acid sequence similarity to PanD from E. coli and Bacillus subtilis, respectively. Subcloning of only this ORF into vectors pBBR1MCS-3 and pBluescript KS- led to complementation of the panD mutants of R. eutropha and E. coli SJ16, respectively. panD-encoded L-aspartate-1-decarboxylase was further confirmed by an enzymatic assay. Upstream of panD, an ORF with strong similarity to pntAA from E. coli, encoding NAD(P)+ transhydrogenase subunit alpha 1 was found; downstream of panD, two ORFs with strong similarity to pntAB and pntB, encoding subunits alpha 2 and beta of the NAD(P)+ transhydrogenase, respectively, were identified. Thus, a hitherto undetermined organization of pan and pnt genes was found in R. eutropha. Labeling experiments using one of the R. eutropha panD mutants and [2-14C]beta-alanine provided no evidence that R. eutropha PHA synthase is covalently modified by posttranslational attachment of 4-phosphopantetheine, nor did the E. coli panD mutant exhibit detectable labeling of functional PHA synthase from R. eutropha. (+info)
H+-zwitterionic amino acid symport at the brush-border membrane of human intestinal epithelial (CACO-2) cells. (2/407)Transport of a number of dipolar amino acids (and the orally active antibiotic D-cycloserine) across the apical membrane of human intestinal epithelial (Caco-2) cell monolayers is mediated by a Na+-independent, pH-dependent transport mechanism. Relatively little is known about the mode of action of this transport system so to differentiate between pH dependence and proton coupling three experimental protocols were designed and tested. The results demonstrate, firstly, that it is the transapical pH gradient and its maintenance (rather than apical acidity alone) that is important in amino acid uptake. Secondly, Na+-independent uptake of seven dipolar amino acids (with pKa (-log of acid dissociation constant) values between 1 50 and 4 23) showed a similar dependence on apical pH (half-maximal uptake being observed at pH 5 99-6 20). Thirdly, the pattern of pH-dependent amino acid ([beta]-alanine) uptake is similar irrespective of whether the cationic substrate concentration is varied or constant, demonstrating no relationship between uptake and concentration of the cationic form of the amino acid. These observations demonstrate that the transport mechanism is a H+-zwitterionic amino acid symporter and suggest that the presence of a H+ gradient at the apical surface of the human small intestine (in the form of the acid microclimate) may be important in driving nutrient absorption. (+info)
Decreased insulin-stimulated GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats. (3/407)It was recently found that the effect of an exercise-induced increase in muscle GLUT-4 on insulin-stimulated glucose transport is masked by a decreased responsiveness to insulin in glycogen-supercompensated muscle. We evaluated the role of hexosamines in this decrease in insulin responsiveness and found that UDP-N-acetyl hexosamine concentrations were not higher in glycogen-supercompensated muscles than in control muscles with a low glycogen content. We determined whether the smaller increase in glucose transport is due to translocation of fewer GLUT-4 to the cell surface with the 2-N-4-(1-azi-2,2,2-trifluroethyl)-benzoyl-1, 3-bis(D-mannose-4-yloxy)-2-propylamine (ATB-[2-3H]BMPA) photolabeling technique. The insulin-induced increase in GLUT-4 at the cell surface was no greater in glycogen-supercompensated exercised muscle than in muscles of sedentary controls and only 50% as great as in exercised muscles with a low glycogen content. We conclude that the decreased insulin responsiveness of glucose transport in glycogen-supercompensated muscle is not due to increased accumulation of hexosamine biosynthetic pathway end products and that the smaller increase in glucose transport is mediated by translocation of fewer GLUT-4 to the cell surface. (+info)
Alterations of intratumoral pharmacokinetics of 5-fluorouracil in head and neck carcinoma during simultaneous radiochemotherapy. (4/407)The kinetics of local drug uptake and metabolism of the anticancer drug 5-fluorouracil (5-FU) has been monitored by means of 19F nuclear magnetic resonance spectroscopy in 17 patients with neck tumors during concurrent radiochemotherapy. All of the patients underwent an accelerated hyperfractionated, concomitant-boost radiochemotherapy with 5-FU [600 or 1000 mg/m2 of body surface (b.s.)] and carboplatin (70 mg/m2 of b.s.). Serial 19F nuclear magnetic resonance spectra were obtained during and after the administration of 5-FU in a 15-T scanner with the use of a 5-cm diameter surface coil positioned on a cervical lymph node metastasis. Examinations were performed at day 1 of therapy and, in 13 patients, also after 43.5 Gy of irradiation at day 1 of the second chemotherapy cycle. Resonances of 5-FU and the catabolites 5,6-dihydro-5-fluorouracil (DHFU) and alpha-fluoro-beta-alanine (FBAL) were resolved in the tumor spectra. The median of the 5-FU and FBAL levels was significantly higher (more than 2-fold) at the second compared with the first examination, whereas the level of DHFU did not change. This effect could indicate an increased delivery of 5-FU into the interstitial space of the tumor in the course of the combined treatment, which would result in an enhanced exposure of the tumor cells to the drug. A potential mechanism for synergy between radio- and chemotherapy is discussed, but alternative mechanisms are also being considered. The findings indicate that a method is available to rationally address the design of dosing schedules in concurrent therapy regimens. (+info)
Role of tyrosine 265 of alanine racemase from Bacillus stearothermophilus. (5/407)Tyrosine 265 (Y265) of Bacillus stearothermophilus is believed to serve as a catalytic base specific to the L-enantiomer of a substrate amino acid by removing (or returning) an alpha-hydrogen from (or to) the isomer on the basis of the X-ray structure of the enzyme [Stamper, C.G., Morollo, A.A., and Ringe, D. (1998) Biochemistry 37, 10438-10443]. We found that the Y265-->Ala mutant (Y265A) enzyme is virtually inactive as a catalyst for alanine racemization. We examined the role of Y265 further with beta-chloroalanine as a substrate with the expectation that the Y265A mutant only catalyzes the alpha,beta-elimination of the D-enantiomer of beta-chloroalanine. However, L-beta-chloroalanine also served as a substrate; this enantiomer was rather better as a substrate than its antipode. Moreover, the mutant enzyme was as equally active as the wild-type enzyme in the elimination reaction. These findings indicate that Y265 is essential for alanine racemization but not for beta-chloroalanine elimination. (+info)
Effect of hypertonic stress on amino acid levels and system A activity in rat peritoneal mesothelial cells. (6/407)OBJECTIVE: Peritoneal mesothelial cells (PMC) are exposed to a hypertonic environment during peritoneal dialysis. When exposed to a hypertonic medium, many types of cells accumulate small osmotically active organic solutes, which are called osmolytes, to match the higher external osmolality. However, no information has been available concerning the osmolytes in PMC. To investigate osmoregulation in rat PMC, the levels of amino acids in the cells and the activity of system A, a major neutral amino acid transport, were measured after switching to a medium made hypertonic by the addition of NaCl. System A was measured by Na+-dependent [14C]-2-methylamino-isobutyric acid (MeAIB) uptake. RESULTS: Total amount of 20 amino acids increased from 306 to 757 nmol/mg protein after 12 hours of hypertonicity. The amount of neutral amino acids accounted for 81% of the increase in total amino acids. Glutamine, alanine, glycine, threonine, and serine were the major neutral amino acids that accumulated in the hypertonic mesothelial cells. The amount of neutral amino acids increased 2.9-fold after 12 hr of hypertonicity, and decreased thereafter. MeAIB uptake increased 36-fold relative to the uptake in isotonic cells after 4-8 hr of hypertonicity. When the culture medium was made hypertonic by adding raffinose or glucose, the activity of system A was also stimulated (raffinose > glucose > NaCl). System A was located on both the apical and basal sides of isotonic PMC, and extracellular hypertonicity stimulated the MeAIB uptake on both sides. CONCLUSIONS: These data indicate that neutral amino acids and system A transport play an important role in early-phase osmoregulation in rat peritoneal mesothelial cells. (+info)
Fibrinogen receptor antagonist-induced thrombocytopenia in chimpanzee and rhesus monkey associated with preexisting drug-dependent antibodies to platelet glycoprotein IIb/IIIa. (7/407)Most clinical trials with fibrinogen receptor antagonists (FRAs) have been associated with thrombocytopenia. This report describes the occurrence of thrombocytopenia in one chimpanzee and one rhesus monkey upon administration of potent FRAs. Chimpanzee A-264 experienced profound thrombocytopenia on two occasions immediately upon intravenous administration of two different potent FRAs, L-738, 167 and L-739,758. However, an equally efficacious antiaggregatory dose of another potent antagonist, L-734,217, caused no change in platelet count. These compounds did not affect platelet count in five other chimpanzees or numerous other nonhuman primates. Flow cytometric analysis showed drug-dependent antibodies (DDAbs) in the plasma of chimpanzee A-264 that bound to platelets of chimpanzees, humans, and all other primates tested only in the presence of the compounds that induced thrombocytopenia. Rhesus monkey 94-R021 experienced thrombocytopenia upon administration of a different antagonist, L-767,679, and several prodrugs that are converted into the active form, L-767,679, in the blood. More than 20 other FRAs, including those that induced thrombocytopenia in chimpanzee A-264, had no effect on platelet count in this monkey. Flow cytometric measurements again identified DDAbs that reacted with platelets of all primates tested and required the presence of L-767,679. Screening for DDAbs in the plasma of 1,032 human subjects with L-738, 167 and L-739,758 demonstrated that the incidence of these preexisting antibodies in this population was 0.8% +/- 0.6% and 1.1% +/- 0.6%, respectively. (+info)
Investigation of the alpha(1)-glycine receptor channel-opening kinetics in the submillisecond time domain. (8/407)The activation and desensitization kinetics of the human alpha(1)-homooligomeric glycine receptor, which was transiently expressed in HEK 293 cells, were studied with a 100-microseconds time resolution to determine the rate and equilibrium constants of individual receptor reaction steps. Concentration jumps of the activating ligands glycine and beta-alanine were initiated by photolysis of caged, inactive precursors and were followed by neurotransmitter binding, receptor-channel opening, and receptor desensitization steps that were separated along the time axis. Analysis of the ligand concentration-dependence of these processes allows the determination of 1) the rate constants of glycine binding, k(+1) approximately 10(7) M(-1) s(-1), and dissociation, k(-1) = 1900 s(-1); 2) the rates of receptor-channel opening, k(op) = 2200 s(-1), and closing, k(cl) = 38 s(-1); 3) the receptor desensitization rate, alpha = 0.45 s(-1); 4) the number of occupied ligand binding sites necessary for receptor-channel activation and desensitization, n >/= 3; and 5) the maximum receptor-channel open probability, p(0) > 0.95. The kinetics of receptor-channel activation are insensitive to the transmembrane potential. A general model for glycine receptor activation explaining the experimental data consists of a sequential mechanism based on rapid ligand-binding steps preceding a rate-limiting receptor-channel opening reaction and slow receptor desensitization. (+info)
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are many different types of liver diseases, including:
1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.
Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.
Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are two main types of fatty liver disease:
1. Alcoholic fatty liver disease (AFLD): This type of fatty liver disease is caused by excessive alcohol consumption and is the most common cause of fatty liver disease in the United States.
2. Non-alcoholic fatty liver disease (NAFLD): This type of fatty liver disease is not caused by alcohol consumption and is the most common cause of fatty liver disease worldwide. It is often associated with obesity, diabetes, and high cholesterol.
There are several risk factors for developing fatty liver disease, including:
* Physical inactivity
* High calorie intake
* Alcohol consumption
* High cholesterol
* High triglycerides
* History of liver disease
Symptoms of fatty liver disease can include:
* Abdominal discomfort
* Loss of appetite
* Nausea and vomiting
* Abnormal liver function tests
Diagnosis of fatty liver disease is typically made through a combination of physical examination, medical history, and diagnostic tests such as:
* Liver biopsy
* Imaging studies (ultrasound, CT or MRI scans)
* Blood tests (lipid profile, glucose, insulin, and liver function tests)
Treatment of fatty liver disease depends on the underlying cause and severity of the condition. Lifestyle modifications such as weight loss, exercise, and a healthy diet can help improve the condition. In severe cases, medications such as antioxidants, fibric acids, and anti-inflammatory drugs may be prescribed. In some cases, surgery or other procedures may be necessary.
Prevention of fatty liver disease includes:
* Maintaining a healthy weight
* Eating a balanced diet low in sugar and saturated fats
* Engaging in regular physical activity
* Limiting alcohol consumption
* Managing underlying medical conditions such as diabetes and high cholesterol.
The excessive production of oxalate can cause a range of symptoms, including kidney stones, damage to the kidneys and other organs, and an increased risk of certain infections. If left untreated, primary hyperoxaluria can lead to serious health problems and may even be fatal.
The exact cause of primary hyperoxaluria is not fully understood, but it is thought to be related to mutations in genes that code for enzymes involved in the production of oxalate. These mutations can be inherited from one or both parents, and the disorder can affect individuals of all ages and backgrounds.
There is currently no cure for primary hyperoxaluria, but various treatments are available to help manage the symptoms and prevent complications. These may include medications to reduce the production of oxalate, dietary changes to limit the intake of oxalate-rich foods, and other supportive measures to help maintain kidney function and overall health.
In summary, primary hyperoxaluria is a rare genetic disorder that affects the liver and causes an excessive amount of oxalate to be produced in the body. This can lead to a range of symptoms and health problems if left untreated, so it is important for individuals with this condition to receive prompt and appropriate medical attention.
There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.
Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.
There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.
Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.
Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.
The condition can be caused by a variety of factors, including excessive alcohol consumption, viral hepatitis, non-alcoholic fatty liver disease, and certain medications. It can also be a complication of other diseases such as hemochromatosis and Wilson's disease.
The symptoms of liver cirrhosis can vary depending on the severity of the disease, but may include fatigue, loss of appetite, nausea, abdominal swelling, and pain in the upper right side of the abdomen. As the disease progresses, it can lead to complications such as esophageal varices, ascites, and liver failure, which can be life-threatening.
There is no cure for liver cirrhosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control swelling and pain, dietary changes, and in severe cases, liver transplantation. In some cases, a liver transplant may be necessary if the disease has caused significant damage and there is no other option to save the patient's life.
In conclusion, liver cirrhosis is a serious and potentially life-threatening condition that can cause significant damage to the liver and lead to complications such as liver failure. It is important for individuals to be aware of the risk factors and symptoms of the disease in order to seek medical attention if they suspect they may have liver cirrhosis. With proper treatment and management, it is possible to slow the progression of the disease and improve the patient's quality of life.
A persistent infection with the hepatitis B virus (HBV) that can lead to liver cirrhosis and hepatocellular carcinoma. HBV is a bloodborne pathogen and can be spread through contact with infected blood, sexual contact, or vertical transmission from mother to child during childbirth.
Chronic hepatitis B is characterized by the presence of HBsAg in the blood for more than 6 months, indicating that the virus is still present in the liver. The disease can be asymptomatic or symptomatic, with symptoms such as fatigue, malaise, loss of appetite, nausea, vomiting, joint pain, and jaundice.
Chronic hepatitis B is diagnosed through serological tests such as HBsAg, anti-HBc, and HBV DNA. Treatment options include interferon alpha and nucleos(t)ide analogues, which can slow the progression of the disease but do not cure it.
Prevention strategies for chronic hepatitis B include vaccination with hepatitis B vaccine, which is effective in preventing acute and chronic HBV infection, as well as avoidance of risky behaviors such as unprotected sex and sharing of needles.
Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.
There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.
Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.
There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.
Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
The symptoms of chronic hepatitis C may be mild or absent, but some people experience fatigue, joint pain, muscle aches, nausea, loss of appetite, and jaundice (yellowing of the skin and eyes).
Chronic hepatitis C is usually diagnosed through blood tests that detect the presence of antibodies against HCV or the virus itself. Imaging tests such as ultrasound and liver biopsy may also be performed to assess the extent of liver damage.
Treatment for chronic hepatitis C typically involves a combination of medications, including interferon and ribavirin, which can help clear the virus from the body. In severe cases, a liver transplant may be necessary. Prevention of the spread of HCV includes avoiding sharing of needles or other sharp objects, practicing safe sex, and getting tested for the virus before donating blood or organs.
See also: Hepatitis C; Liver; Virus
There are several types of hepatitis C, including genotype 1, which is the most common and accounts for approximately 70% of cases in the United States. Other genotypes include 2, 3, 4, 5, and 6. The symptoms of hepatitis C can range from mild to severe and may include fatigue, fever, loss of appetite, nausea, vomiting, joint pain, jaundice (yellowing of the skin and eyes), dark urine, pale stools, and itching all over the body. Some people with hepatitis C may not experience any symptoms at all.
Hepatitis C is diagnosed through a combination of blood tests that detect the presence of antibodies against HCV or the virus itself. Treatment typically involves a combination of medications, including interferon and ribavirin, which can cure the infection but may have side effects such as fatigue, nausea, and depression. In recent years, new drugs known as direct-acting antivirals (DAAs) have become available, which can cure the infection with fewer side effects and in a shorter period of time.
Prevention measures for hepatitis C include avoiding sharing needles or other drug paraphernalia, using condoms to prevent sexual transmission, and ensuring that any tattoos or piercings are performed with sterilized equipment. Vaccines are also available for people who are at high risk of contracting the virus, such as healthcare workers and individuals who engage in high-risk behaviors.
Overall, hepatitis C is a serious and common liver disease that can lead to significant health complications if left untreated. Fortunately, with advances in medical technology and treatment options, it is possible to manage and cure the virus with proper care and attention.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
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- Increasing carnosine levels through Beta Alanine supplementation may delay fatigue during endurance exercise or translate into lifting more weights and increasing total work output. (lky7sports.com)
- One study looked at the effect of beta-alanine supplementation and muscle carnosine concentrations on the performance of highly trained rowers. (clubvits.com)
- Before supplementation the placebo group was 0.3 seconds quicker, however after the supplementation those taking beta-alanine were 4.3 seconds quicker. (clubvits.com)
- A study using 400m sprint trained athletes found that beta-alanine supplementation significantly increased muscle carnosine levels. (clubvits.com)
- The real benefit is experienced following several weeks of daily supplementation as it takes time to build up and saturate your muscles beta-alanine stores. (clubvits.com)
- β-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters. (clubvits.com)
- Clinical studies suggest that Beta-Alanine supplementation can help delay muscle fatigue for increased endurance during exercise. (vitaminherbstore.com)
- After a few weeks of supplementation with Beta-Alanine, this sensation normally lessens or subsides. (vitaminherbstore.com)
- Research studies have shown that Beta-Alanine supplementation not only can boost performance but also support increases in lean muscle mass. (monsterzym.com)
- Beta-alanine supplementation has become popular in recent years, as it is thought to increase muscle carnosine levels and improve exercise performance. (supplementsguide.co)
- However, one of the side effects of beta-alanine supplementation is a condition known as paresthesia, which is characterized by a tingling or prickling sensation on the skin. (supplementsguide.co)
- While the tingling sensation caused by beta-alanine supplementation may be uncomfortable for some, it is generally harmless and will subside once supplementation is stopped. (supplementsguide.co)
- The good news is that the beta-alanine itch is generally harmless and will subside once supplementation is stopped. (supplementsguide.co)
- If you're new to beta-alanine supplementation, it's best to start with a lower dose and increase it gradually over time. (supplementsguide.co)
- The most common side effect of beta-alanine supplementation is the beta-alanine itch, which is a tingling or prickling sensation on the skin. (supplementsguide.co)
- Beta-Alanine supplementation can increase muscle Carnosine content and delay muscle fatigue. (fitshop.ca)
- The neurotoxin β-N-methylamino-L-alanine (BMAA), a non-proteinogenic amino acid produced by several species of both prokaryotic (cyanobacteria) and eukaryotic (diatoms) microorganisms, has been proposed to be associated with the development of neurodegenerative diseases. (mdpi.com)
- Beta-Alanine is an amino acid which has become very popular in the world of sports nutrition as research has shown that it improves muscular endurance. (clubvits.com)
- When ingested beta alanine binds with the amino acid histidine to produce an acidity buffer known as Carnosine. (clubvits.com)
- The chemical reactions and pathways resulting in the breakdown of beta-alanine (3-aminopropanoic acid), an achiral amino acid and an isomer of alanine. (tamu.edu)
- Beta-Alanine is a non-essential amino acid naturally produced in muscle cells. (vitaminherbstore.com)
- Beta-alanine is a naturally occurring amino acid that is classified as a non-essential amino acid. (supplementsguide.co)
- Tested Beta Alanine is a non-essential amino acid that is converted to carnosine by the muscle cells. (fitshop.ca)
- Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. (nih.gov)
- The results of studies on beta-alanine, an amino acid found in food and dietary supplements, are mixed but generally don't show that it improves athletic performance significantly. (nih.gov)
- Along with creatine, BCAA's and caffeine, beta-alanine has become a staple of pre-workout supplements. (clubvits.com)
- Although beta-alanine is often taken before training and is incorporated into many pre-workout supplements it can be taken at any time throughout the day. (clubvits.com)
- Beta Alanine_Dietary supplements ingredients, vitamins and minerals. (health-sources.com)
- pouze od takov ch u ivatel , kte v na em obchod Beta Alanine 1000 zakoupili a pot k n mu napsali recenzi. (ronnie.cz)
- Amino acids are the building blocks of proteins, and beta-alanine is used by muscles to synthesize carnosine. (supplementsguide.co)
- As a byproduct, beta alanine can also decrease fatigue while training and increase total workload. (elitefts.com)
- Research suggests that supplementing with 4-6 grams of beta-alanine daily for 28 days can lead to a 40-60 percent increase in carnosine concentrations. (bodybuilding.com)
- If you're not a fan of the tingling sensation you can get when you take larger doses of beta-alanine, split them into smaller doses of 1.6 grams. (bodybuilding.com)
- The recommended dosage of beta-alanine is 2-5 grams per day. (supplementsguide.co)
- In fact, the typical dose of beta-alanine used in most pre-workouts is far too little to have any immediate effect on performance, which is why you have to take it every day and give it time to build up inside your system. (bodybuilding.com)
- The standard daily dose of beta-alanine is between 3-6 g. (clubvits.com)
- Olimp Beta-alanine Carno Rush Mega Tabs ® - a specially-designed combination of beta-alanine, l-histidine and vitamin B6! (beingbuilder.com)
- Beta-alanine and L-histidine supplemented together provide two substances necessary for the synthesis of carnosine, which shows great anti-oxidizing potential and may delay degrading processes in the cells during intense workouts. (beingbuilder.com)
- Three pathways were significantly perturbed in exposed workers and had an impact score >0.5: beta-alanine metabolism, histidine metabolism, and glycine, serine, and threonine metabolism. (cdc.gov)
- Nutricost Beta-Alanine Capsules 3400mg, 24. (fakespot.com)
- 5. Brown adipose tissue transcriptome unveils an important role of the Beta-alanine/alamandine receptor, MrgD, in metabolism. (nih.gov)
- Al haberse demostrado la captación neuronal y la sensibilidad receptora neuronal a la beta-alanina, el compuesto puede ser un transmisor falso, sustituto del ÁCIDO GAMMA AMINOBUTÍRICO. (bvsalud.org)
Tingling sensation on the skin1
- Beta-Alanine may cause a harmless, temporary tingling sensation on the skin for some individuals. (vitaminherbstore.com)
- Food sources such as beef and chicken contain beta-alanine however only in small doses. (clubvits.com)
- Some companies may put a gram or two of beta-alanine into pre-workouts just to give you an instant physical sensation. (bodybuilding.com)
- When levels of beta-alanine and carnosine become too high, they begin to interact with nerve endings in the skin, causing the tingling sensation. (supplementsguide.co)
- Boost your performance by learning how to supplement with beta-alanine the right way! (bodybuilding.com)
- If you're going to supplement with beta-alanine, here's what you need to know about this widely used, but poorly understood, ingredient. (bodybuilding.com)
- The availability of beta-alanine is the limiting factor when it comes to carnosine production therefore taking it in supplement form will allow more carnosine to be formed. (clubvits.com)
- Olimp Beta-alanine Carno Rush Mega Tabs® is a supplement designed for all who practice strength-endurance sports, strength sports and endurance sports that require great physical fitness mai. (beingbuilder.com)
- Olimp Beta-alanine Carno Rush Mega Tabs ® is a supplement designed for all who practice strength-endurance sports, strength sports and endurance sports that require great physical fitness maintained for a longer period of time, or have a great frequency of training sessions. (beingbuilder.com)
- Additionally, beta-alanine has been shown to be a safe and effective supplement for improving exercise performance. (supplementsguide.co)
- So, if you're looking for a supplement that can help you train harder and longer, beta-alanine may be a good option for you. (supplementsguide.co)
- If you've ever taken a beta-alanine supplement, chances are you've experienced the "beta-alanine itch. (supplementsguide.co)
- This will help your body to adjust to the supplement and minimize the chances of experiencing the beta-alanine itch. (supplementsguide.co)
- 18 rowers supplemented with 5g/day of either a placebo or beta-alanine for 7 weeks. (clubvits.com)
- This increase in acidity impairs the muscles ability to contract with force… this is where beta-alanine comes in. (clubvits.com)
- In fact, a 2017 survey of 570 athletes who took beta-alanine found that 65 percent of them couldn't identify its benefits , and only 12 percent took it every day as recommended. (bodybuilding.com)
- Buy Tested Nutrition Beta-Alanine (180 Caps) for Less! (fitshop.ca)
- Ogfod1 deletion increases cardiac beta-alanine levels and protects mice against ischemia-reperfusion injury. (nih.gov)
- In one study, athletes who consumed both creatine and beta-alanine demonstrated better endurance than those who took only one. (bodybuilding.com)
- A second study found that athletes who followed a 10-week resistance-training program and supplemented with creatine and beta-alanine saw greater improvements in muscle mass and body fat. (bodybuilding.com)
- Beta-alanine is one of those ingredients that seems to find its way into just about every pre-workout on the market. (bodybuilding.com)
- Olimp Beta-alanine Carno Rush Mega Tabs ® helps to prolong the time before becoming tired, thus increasing the workout volume significantly. (beingbuilder.com)
- Beta Alanine is ideal for anyone participating in explosive sports (such as weightlifting) or those involved in prolonged endurance exercise. (lky7sports.com)
- 1] Most of the athletes also grossly underestimated the time required for beta-alanine to take effect. (bodybuilding.com)
- Or you can choose products with the sustained-release form of beta-alanine, which has the same effect of increasing carnosine stores, but with little or no tingling. (bodybuilding.com)
- Cases of pulmonary arterial hypertension (PAH) have been reported in patients treated with interferon beta products, including EXTAVIA. (nih.gov)
- The exact mechanism by which beta-alanine causes paresthesia is not fully understood, but it is thought to be due to the accumulation of beta-alanine and carnosine in the bloodstream. (supplementsguide.co)
- This side effect is caused by the accumulation of beta-alanine and carnosine in the bloodstream. (supplementsguide.co)
- PrimaForce™ Beta-Alanine helps users train harder for longer. (monsterzym.com)
- A Guide to Beta-Alanine. (clubvits.com)